MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.
The recently discovered peptide editor TAPBPR binds to UDP-glucose:glycoprotein glucosyltransferase 1 to provide quality control in the antigen presentation pathway by facilitating the reglucosylation of the glycan on MHC class I molecules.
A multi-transcriptional CDKs inhibitor suppresses MYC and induces regression of ovarian tumors, indicating that targeting CDK7, 12, 13 with THZ1 may be an effective approach for treating MYC-dependent malignancies.
The number of different peptides presented by major histocompatibility complex class I molecules to the immune system's T lymphocytes is inversely correlated with cell surface expression and is strongly associated with the response to infectious disease.
A generally applicable two-hybrid assay demonstrates that MHC class I heavy chains devoid of beta-2 microglobulin associate within and across allotypes, with implications for endocytosis and autoimmunity.